Relevance of mitochondrial alterations in the neurodegenerative diseases, an update and discussion of evidence

• Published in: Revista mexicana de neurociencia Vol. 24; no. 4; pp. 117 - 125
• Main Authors: Aguilar-Gamas, Carlos F., Martínez-Abundis, Eduardo, Gómez-Crisóstomo, Nancy P., de la Cruz-Hernández, Erick N.
• Format: Journal Article
• Language: English; Portuguese
• Published: Academia Mexicana de Neurología A.C 01.10.2023; Permanyer
• Subjects: Clinical Neurology; Neurodegenerative disease. Mitochondrial dysfunction. Alzheimer disease. Parkinson disease. Huntington disease; Neurosciences; Enfermedad de Parkinson; Mitochondrial dysfunction; Alzheimer disease; Huntington disease; Enfermedad de Huntington; Parkinson disease; Enfermedad neurodegenerativa; Neurodegenerative disease; Enfermedad de Alzheimer; Disfunción mitocondrial
• ISSN: 2604-6180; 2604-6180
• DOI: 10.24875/RMN.23000006

Abstract Neurodegenerative diseases (ND) are undoubtedly part of the more important health issues worldwide. The loss of independence and decreased quality of life are characteristics of these patients that translate into an economic load on relatives and health services. Although myriad factors or metabolic alterations are blamed as causatives, there is a common defect in almost every ND, mitochondrial dysfunction. Mitochondria are the cell’s leading energy supplier; therefore, altering its function will affect the cellular function with the energy demand. Defects in mitochondrial mechanisms such as ATP synthesis by the mitochondrial respiratory chain, mitochondrial dynamics, apoptosis regulation, and oxidative stress are described as part of the pathological characteristics of Alzheimer’s, Parkinson’s, Huntington’s diseases, and Amyotrophic Lateral Sclerosis. In this review, we will briefly describe the mitochondrial roles in cell life before analyzing the recently published bibliography that addresses the mitochondrial dysfunction and mitochondrial mechanisms implicated in ND and will discuss a relevant question in the field: is mitochondrial dysfunction a cause or consequence for these diseases?